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Background: Currently there is no consensus regarding which add-on therapy to use in resistant hypertension. This study was designed to compare two treatment options, spironolactone (SPR) versus dual blockade of the renin-angiotensin-aldosterone system (RAAS)., Methods: Forty-two patients with true resistant hypertension were included in the study. An open-label prospective crossover design was used to add a second RAAS blocker to previous treatment and then SPR following 1 month of wash-out. BP was measured in the office and by ambulatory blood pressure monitoring (ABPM). Changes in laboratory tests were also studied for both treatments. The predictive values of aldosterone-renin ratio (ARR) and serum potassium of determining the antihypertensive response were analyzed for both arms., Results: Following the first stage of dual blockade, SBP dropped significantly both in office (reduction of 12.9 ± 19.2 mmHg)) and by ABPM (reduction of 7.1 ± 13.4 mmHg). Office DBP was unchanged but was significantly reduced as measured by ABPM (3.4 ± 6.2 mmHg). On SPR treatment, office BP was reduced 32.2 ± 20.6/10.9 ± 11.6 mmHg. By ABPM the reduction was 20.8 ± 14.6/8.8 ± 7.3 mmHg (P < 0.001). The BP control was achieved by 25.6% of patients in dual blockade and 53.8% in SPR with office blood pressure. By ABPM, 20.5% were controlled on dual blockade and up to 56.4% with SPR. Serum potassium was a weak inverse predictor of the blood pressure-lowering effect of SPR., Conclusion: SPR has a greater antihypertensive effect than dual blockade of the RAAS in resistant hypertension. SPR at daily doses of 25-50 mg shows a potent antihypertensive effect when added to prior regimes of single RAAS axis blockade in patients with resistant arterial hypertension.

Objective: To investigate the influence of metabolic syndrome (MS) on risk stratification and ulterior classification in hypertensive patients at entry into a hypertension unit by comparing the criteria of ESH-ESC 2003 and 2007 guidelines., Methods: 720 consecutive patients attending a hospital-located hypertension unit were included in the study. They were classified with or without MS according to the ATP-III 2005 report. Patients underwent repeated office BP measurements and routine blood/urine examinations. In addition ultrasensitive CRP (uCRP), echocardiogram, fasting insulin, urinary albumin excretion were determined and HOMA index was calculated., Results: The prevalence of MS was 58.8 %. Abdominal obesity and fasting glucose were the most prevalent components of MS, and HDL-cholesterol the least prevalent. MS group had higher levels of LDL-cholesterol and higher prevalence of left ventricular hypertrophy and microalbuminuria. Patients with MS also presented a significant elevation in uCRP, fasting insulin and HOMA. BP was controlled in 55.6%. When we applied the 2003 guideline, 48.9% patients showed a high or very high added cardiovascular risk. With the applications of the 2007 guide the prevalence of this two categories reach 73.9%., Conclusions: A significant difference in the risk pattern distribution is found when MS is considered in risk stratification in our hypertensive population. The accompanying increase in the levels of other cardiovascular risk factors and in the prevalence of target organ damage justifies the global intervention on cardiovascular risk recommended by 2007 ESH-ESC guidelines.

Background: Even with optimal blood pressure control, organ protection may also depend on the selected therapeutic regime. Angiotensin-converting enzyme inhibitors have been shown to provide excellent organ protection in hypertension, and may show dose-dependent protective effects. Adrenergic alpha blockers have been associated with an increased rate of heart failure in the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) and Vasodilator-Heart Failure Trial (V-HeFT). This has been related to a proapoptotic effect of this drug in cardiomyocytes. Our purpose is to compare the heart and renal protection of a high quinapril dose, with a combined low quinapril dose plus doxazosin, in an animal model of chronic hypertension., Methods: Uninephrectomized spontaneously hypertensive 12-week-old rats were treated for 36 weeks with either quinapril or a combination of doxazosin plus a low quinapril dose. Tight blood pressure control was achieved with both treatments. Renal and cardiac protection was assessed by different parameters, and cardiac apoptosis was evaluated by active caspase-3, apoptotic protein and heat shock protein levels. Untreated hypertensive and normotensive rats were included as controls., Results: Both treatments showed significant heart and renal protection compared with untreated animals. Both therapeutic regimes showed similar protection in renal and cardiac pathology, coronary media fibrosis, myocardial apoptosis and cardiac index. Proteinuria and left ventricular hypertrophy regression were significantly lower in the quinapril group compared with the combined treatment group., Conclusions: Blood pressure control with a high quinapril dose provided higher organ protection than a combined therapy with a lower quinapril dose. This effect was not due to a deleterious effect of doxazosin.

Left ventricular hypertrophy increases the risk for cardiovascular target organ damage, myocardial infarction, and stroke. The authors assessed the patterns of ventricular adaptation in 107 essential hypertensives whose treatment had been withdrawn and its modification after 1 year of hypertension treatment. Blood pressure decreased from 158+/-17/96+/-12 mm Hg to 137+/-15/83+/-10 mm Hg (mean +/- SD; p<0.001); 45% of the patients (49 of 107) had their blood pressure controlled below 140 mm Hg and 90 mm Hg. Although a significant decrease of left ventricular mass index was found in the study, the percentage of patients with normal left ventricular geometry at the completion of the study increased by only 9% (27% to 36%, p>0.05). Left ventricular mass geometry improved in 31% of the patients, remained unaffected in 51%, and worsened in 18%. The data suggest that even while suboptimal antihypertensive treatment reduces left ventricular mass index, either left ventricular hypertrophy or concentric remodeling remains present in a significant number of patients at the end of a 1-year treatment period. The authors conclude that these patients should be considered as a subgroup at high risk and should be treated more aggressively.

Objective: To determine causes of treatment resistance in patients with refractory hypertension, and to estimate the prevalence of true resistant hypertension. Methods: We studied 50 consecutive patients referred with refractory hypertension after exclusion of hypokalemia and stenosis of the renal artery. Ambulatory blood pressure monitoring was performed in all patients to detect white-coat effect. The patients were hospitalized, antihypertensive drugs were withdrawn and a screening for secondary hypertension was performed. In addition, these patients, and a control group of essential hypertensives controlled with three antihypertensive drugs, underwent a OGTT with 75 g of glucose. Results: Primary normokaliemic hyperaldosteronism was diagnosed in seven patients. Two patients had a pheochromocytoma and six had white-coat effect. The 35 remaining patients with true resistant hypertension shown significant differences in serum insulin and HOMA IR when compared with the control group. Conclusions: These findings show that among normokaliemic treatment-resistant hypertension, the presence of hyperaldosteronism and pheochromocitoma is quite high. Moreover, treatment resistance in hypertensive patients appears to be associated with insulin resistance. [ABSTRACT FROM AUTHOR]